Macular Degeneration: Zambarakji H

Marneros AG, She H, Zambarakji H, Hashizume H, Connolly EJ, Kim I, Gragoudas ES, Miller JW, Olsen BR. · Department of Developmental Biology, Harvard School of Dental Medicine, 188 Longwood Ave., Boston, MA 02115, USA. · FASEB J. · Pubmed #17526870 links to  free full text

Abstract: Endostatin, a fragment of the basement membrane component collagen XVIII, exhibits antiangiogenic properties in vitro and in vivo when high doses are administered. It is not known whether endogenous endostatin at physiological levels has a protective role as an inhibitor of pathological angiogenesis, such as choroidal neovascularization (CNV) in age-related macular degeneration. Using a laser injury model, we induced CNV in mice lacking collagen XVIII/endostatin and in control mice. CNV lesions in mutant mice were approximately 3-fold larger than in control mice and showed increased vascular leakage. These differences were independent of age-related changes at the choroid-retina interface. Ultrastructural analysis of the choroidal vasculature in mutant mice excluded morphological vascular abnormalities as a cause for the larger CNV lesions. When recombinant endostatin was administered to collagen XVIII/endostatin-deficient mice, CNV lesions were similar to those seen in control mice. In control mice treated with recombinant endostatin, CNV lesions were almost undetectable. These findings demonstrate that endogenous endostatin is an inhibitor of induced angiogenesis and that administration of endostatin potently inhibits CNV growth and vascular leakage. Endostatin may have a regulatory role in the pathogenesis of CNV and could be used therapeutically to inhibit growth and leakage of CNV lesions.

Tranos P, Scott R, Zambarakji H, Zambarajki H, Ayliffe W, Pavesio C, Charteris DG. · Department of Vitreoretinal Surgery, Moorfields Eye Hospital, London, EC1V 2PD, UK. · Br J Ophthalmol. · Pubmed #16723360 No free full text.

Abstract: AIM: To evaluate the efficacy of pars plana vitrectomy (PPV) in the management of chronic uveitic cystoid macular oedema (CMO). METHODS: A prospective, interventional, randomised, controlled, pilot study. 23 eyes of 23 patients with CMO secondary to chronic intermediate or posterior uveitis unresponsive to medical treatment were randomised into a surgical (group S) or medical group (group M). 12 patients in group S underwent PPV as opposed to 11 patients in group M who received systemic corticosteroid and/or immunosuppressive treatment during the study period. The primary outcome measures of the study were change in visual acuity and angiographic appearance of CMO at 6 months. RESULTS: Mean visual acuity in group S improved significantly from 1.0 (0.62) at baseline to 0.55 (0.29) at 6 months following vitrectomy (p = 0.011), with five (42%) eyes reaching vision of 20/40 or better. Conversely, mean visual acuity in group M improved only marginally by 0.03 (0.27) (p = 0.785). CMO after vitrectomy was angiographically improved in four (33%) eyes, remained unchanged in seven (58%) eyes, and deteriorated in one (8%) eye. In the medical group, fluorescein leakage decreased in one eye, did not alter in four eyes, and deteriorated in two eyes. CONCLUSION: PPV for macular oedema secondary to chronic uveitis despite angiographic improvement in only one third of the patients, seems to have a significant beneficial effect on visual function. This study provides enough evidence to justify a large scale trial which would define the role of vitrectomy in uveitic macular oedema.